It is widely accepted that oxidative stress plays a central role in alcohol-induced pathogenesis. The protective effect of
binaphthyl diselenide (
NapSe)2 was investigated in
ethanol (Etoh)-induced
brain injury. Thirty male adult Wistar rats were divided randomly into five groups of six animals each and treated as follows: (1) The control group received the vehicle (
soy bean oil, 1 mL/kg, p.o.). (2)
Ethanol group of animals was administered with
ethanol (70% v/v, 2 mL/kg, p.o.). (3) (
NapSe)2 1 mg/kg, 1 mL/kg plus
ethanol 70% (v/v, 2 mL/kg, p.o. (5) (
NapSe)2 10 mg/kg, 1 mL/kg) plus
ethanol 70% (v/v, 2 mL/kg, p.o). After acute treatment, all rats were sacrificed by
decapitation. Evidence for oxidative stress in rat brain was obtained from the observed levels of
thiobarbituric acid reactive species, of non-
protein thiol (NPSH) groups, and of
ascorbic acid, as well as from the activities of
catalase (CAT) and of
superoxide dismutase (SOD). (
NapSe)2 compensated the deficits in the
antioxidant defense mechanisms (CAT, SOD, NPSH, and
ascorbic acid), and suppressed lipid peroxidation in rat brain resulting from Etoh administration. It was concluded that
ethanol exposure causes alterations in the
antioxidant defense system and induces oxidative stress in rat brain. (
NaPSe)2 at 5 mg/kg restored the
antioxidant defenses in rat brain and mitigated the toxic effects of alcohol, suggesting that could be used as a potential therapeutic agent for alcohol-induced oxidative damage in rat brain.